DEEP VENOUS THROMBOSIS

Venous thromboembolism (VTE) A condition in which a blood clot (thrombus) forms in a vein, which in some cases then breaks free and enters the circulation as an embolus, finally lodging in and completely obstructing a blood vessel, e.g., in lungs causing a PE

The most common type of venous thromboembolism is deep vein thrombosis, which occurs in veins deep within the muscles of the legs,arms and pelvis.

A superficial venous thrombosis (also called phlebitis or superficial thrombophlebitis) is a blood clot that develops in a vein close to the surface of the skin. These types of blood clots do not usually travel to the lungs unless they move from the superficial system into the deep venous system first.

Introduction

Deep vein thrombosis is the formation of a blood clot in one of the deep veins of the body, usually in the leg

Definition

DVT usually originates in the lower extremity venous level ,starting at the calf vein level and progressing proximally to involve popliteal ,femoral ,or iliac system.

.80 -90 % pulmonary emboli originates here .

ETIOLOGY

Virchow describes the three broad categories of factors that are thought to contribute to thrombosis

venous stasis, endothelial damage, hypercoagulable state

Virchow triad

It Occurs in case of- prolonged bed rest (4 days or more) A cast on the leg Limb paralysis from stroke or spinal cord

injury extended travel in a vehicle

Venous stasis

Surgery and trauma (responsible for up to 40% of all thromboembolic disease) injury which damages veins, or surgery can slow down the flow of blood, thus raising the chances of blood clots. General anesthetics can dilate the veins, which makes it more likely that blood pools and clots form.

Malignancy-some types are associated with a higher risk of DVT, as are some cancer therapies.

Increased estrogen (due to a fall in protein ‘S) Increased estrogen occurs during

all stages of pregnancy—the first three months postpartum, after elective abortion, and during treatment with oral contraceptive pills

Hypercoagulability

Congenital Deficiency of anti-thrombin III, protein C or proteinS

Antiphospholipid antibody or lupus anticoagulant

Factor V Leiden gene defect or activated protein C resistance

Dysfibrinogenaemias Acquired Antiphospholipid antibody or lupus

anticoagulant

Abnormalities of thrombosis and fibrinolysis that lead to an increased risk of venous thrombosis

Trauma, surgery, and invasive procedure may disrupt venous

integrity Iatrogenic causes of venous thrombosis are

increasing due to the widespread use of central venous catheters, particularly subclavian and internal jugular lines.

These lines are an important cause of upper extremity DVT, particularly in children.

Endothelial Injury

The beginning of venous thrombosis is thought to be caused by tissue factor, which leads to conversion of prothrombin to thrombin, followed by fibrin deposition. The fibrin appears to attach to the endothelial lining , a surface that normally acts to prevent clotting.

When a clot forms, the coagulation cascade promotes clot growth proximally. Thrombus can extend from the superficial veins into the deep system from which it can embolize to the lungs.

Clinical Pathophysiology

• Opposing the coagulation cascade is the endogenous fibrinolytic system. After the clot organizes or dissolves, most veins will recanalize in several weeks. Residual clots retract.

• But in presence of risk factors this clot propagates proximally and may lodge an emboli to lung

• Residual clots and venous hypertension due to narrowing of lumen may destroy valves, leading to the postphlebitic syndrome, which develops within 5-10 years,

• Edema , sclerosis, and ulceration characterize this syndrome, which develops in 40-80% of patients with DVT.

An organised thrombus. C, clot; T, thrombus

In the majority of cases, only one leg is affected. However, on rare occasions both legs may have a DVT.

Calf pain or tenderness, or both The skin of the affected leg may feel warm Swelling below knee in distal deep vein

thrombosis and up to groin in proximal deep vein thrombosis

Superficial venous dilatation The skin may go red, especially below the

knee behind the leg. The skin may be discolored.

Cyanosis can occur with severe obstruction Leg fatigue

Presentation And Clinical Examination

Palpate distal pulses and evaluate capillary refill to assess limb perfusion.

Move and palpate all joints to detect acute arthritis or other joint pathology.

Homans'’ sign: pain in the posterior calf or knee with forced dorsiflexion of the foot while the knee is fully extended. This is not a commonly used test and should not be done. This test is less used today because it can potentially dislodge the deep vein thrombosis (DVT) and travel to the lung.

examin for signs suggestive of underlying predisposing factors

D- dimer measurement where the well score is longer than 4 or there is clinical suspicion

Investigation

variable Points

Clinical sigs and symptoms of DVT (minimum of leg swelling and pain on palpation of deep veins)

3.0

Alternative diagnosis less likely than PE

3.0

Heart rate >100 1.5

Immobilisation > or surgery within past 4 weeks

1.5

Previous DVT or PE 1.5

Haemoptysis 1.0

Malignanacy (treatment or palliation within past 6 months )

1.0

Modified well’s criteria for predicting pulmonary embolism

If this is greater than the normal range there is no indication for further investigation

But if raised, a duplex compression ultrasound is performed

The deep veins of the lower limb are located and compressed.

Filling defects in flow and a lack of compressibility indicate the presence of a thrombosis

This is accurate for femoral and popliteal clots but less certain in tibial vein clot.

A longitudinal (a) and transverse (b) section of a duplexscan of a vein containing a thrombus

Ascending venography, which shows a thrombus as a filling defect, is now rarely required unless other measures are being considered

An ascending venogram of a deep vein thrombosis seen as filling defects (arrows) with contrast passing around the thrombus

Pulmonary embolism is diagnosed by CT scanning of pulmonary arteries as it can show filling defects in the arteries

Pulmonary angiography is rarely required unless interventional treatment is being considered.

Radionucliotide imaginging has been supersided by CT pulmonary angiography n should not normaly be used.

ruptured Baker’s cyst a calf muscle haematoma a ruptured plantaris muscle a thrombosed popliteal aneurysm and Arterial ischemia

Differential diagnosis of a deep vein thrombosis includes

Patients who are being admitted for surgery can be graded as low,moderate or high risk.

Patients in medium or high risk groups should be considered for anticoagulation prophylaxis

Prophylaxis

Low Minor surgery <30 mins . Any age. No risk factors Major surgery >30 mins. Age <40. no other risk factors Minor trauma or medical illness, any age. no risk factors

Moderate Major surgery. Age 40+ other risk factorsMajor medical illness:heart/lung disease,cancer,inflamatory bowel ds

Major trauma/burns

Minor surgery,trauma,medical illness in patient with previous Dvt,PE or thrombophilia

High Major orthopaedic surgery or fracture pelvis,hip,lower limbMajor abdominal/pelvic surgery for cancerMajor surgery,trauma,medical illness in patient with Dvt,PE or thrombophilia Lower limb paralysis( eg. Stroke,paraplegia)Major lower limb amputation

Risk groups

Prophylactic methods are-

Mechanical Use of graduated

elastic compression stockings and external pneumatic compression have shown reduced incidence of thrombosis

Pharmacological

More effective than mechanical but has risk of bleeding

Heparin is given subcutaneously. Dose dependent on patients weight

No monitoring for dose required and has reduced risk of heparin induced thrombocytopenia

A combination of pharmacological and mechanical treatment with heparin can be used in patients considered at high risk.

Patients in medium n high risk groups should be considered for anticoagulation prophylaxis

Heparin can be given once a day and has lower risk of bleeding complications

Patients who are confirmed to have a deep vein thrombosis on duplex imaging should be started on subcutaneous low molecular weight heparin and rapidly anticoagulated with warfarin unless there is a specific contraindication.

Warfarin is usually started at a dose of 10 mg on day one, 10 mg on day two and 5 mg on day three.

A prothrombin time taken on day three guides the maintenance dose of warfarin.

Treatment of a deep vein thrombosis

Thrombo lysis should be considered, however,in patients with an iliac vein thrombosis, especially if they are seen early and the limb is extremely swollen.

Very few surgeons still carry out venous thrombectomy, although it may still be attempted in patients with pre-venous gangrene

A venous thrombectomy should be accompanied by an arteriovenous fistula to increase venous flow through the vein that has had the thrombus removed.

During thrombo lysis the tissue plasminogen activator in most patients is administered directly into the thrombus, either via the popliteal vein or by direct puncture in the groin.

also New devices are being marketed that physically disrupt the thrombus at the same time as local lysis is carried out.

Some thrombi can be compressed by stent grafting, allowing the venous lumen to be opened, especially in the iliac region.

This technique is very good in patients with an anatomical obstruction from an ‘iliac vein compression syndrome.

Most pulmonary emboli can be treated by anticoagulation and observation but severe right heart strain and shortness of breath indicates the need for fibrinolytic treatment.

Rarely, patients who are on the point of cardiac arrest should undergo surgical pulmonary embolectomy.

Treatment of pulmonary embolus

The term ‘thrombophlebitis’implies a major inflammatory component; however, this is rarely seen.

Common causes include external trauma(especially to varicose veins), venepunctures and infusions ofhyperosmolar solutions and drugs.

The presence of an intravenous cannula for longer than 24–48 hours often leads to thrombosis.

Some systemic diseases such as thromboangiitis obliterans (Buerger’s disease) and malignancy, especially of the pancreas, can lead to a flitting thrombophlebitis, affecting different veins at different times.

Finally, coagulation disorders such as polycythaemia, thrombocytosis and sickle cell disease are often associated, as is a concomitant thrombosis within the deep veins

Superficial thrombophlebitis

The surface vein feels solid and is tender on palpation. The overlying skin may be attached and in the early stages may be erythematous before gradually turning brown.

A linear segment of vein of variable length can be easily palpated once the inflammation has died down.

A full blood count, coagulation screen and duplex scan of the deep veins should usually be obtained.

Any suggestion of an associated malignancy should be investigated using appropriate endoscopy and imaging studies, such as an abdominal CT scan.

Most patients are treated with non-steroidal anti-inflammatory drugs and the condition resolves spontaneously.

Rarely, infected thrombi require incision or excision.

Ligation to prevent propagation into the deep veins is almost never required.

Associated deep vein thrombosis or thrombophilias are treated by anticoagulation.